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Article: Activating TCR signaling to thwart T-all

TitleActivating TCR signaling to thwart T-all
Authors
Issue Date2016
Citation
Cancer Discovery, 2016, v. 6, n. 9, p. 946-948 How to Cite?
Abstract© 2016 American Association for Cancer Research. Thymic negative selection is a process that aims to eliminate autoreactive T cells by inducing the apoptosis of thymocytes expressing a T-cell receptor (TCR) with high affinity for self-MHC. In this issue, Trinquand and colleagues demonstrate that TCR engagement or anti-CD3 stimulation of TCR-expressing T acute lymphoblastic leukemia cells results in their apoptosis. This cell death is reminiscent of thymic negative selection and has the potential for therapeutic exploitation.
Persistent Identifierhttp://hdl.handle.net/10722/292998
ISSN
2023 Impact Factor: 29.7
2023 SCImago Journal Rankings: 7.533
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLemonnier, François-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:57:39Z-
dc.date.available2020-11-17T14:57:39Z-
dc.date.issued2016-
dc.identifier.citationCancer Discovery, 2016, v. 6, n. 9, p. 946-948-
dc.identifier.issn2159-8274-
dc.identifier.urihttp://hdl.handle.net/10722/292998-
dc.description.abstract© 2016 American Association for Cancer Research. Thymic negative selection is a process that aims to eliminate autoreactive T cells by inducing the apoptosis of thymocytes expressing a T-cell receptor (TCR) with high affinity for self-MHC. In this issue, Trinquand and colleagues demonstrate that TCR engagement or anti-CD3 stimulation of TCR-expressing T acute lymphoblastic leukemia cells results in their apoptosis. This cell death is reminiscent of thymic negative selection and has the potential for therapeutic exploitation.-
dc.languageeng-
dc.relation.ispartofCancer Discovery-
dc.titleActivating TCR signaling to thwart T-all-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/2159-8290.CD-16-0789-
dc.identifier.pmid27587465-
dc.identifier.scopuseid_2-s2.0-85012022683-
dc.identifier.volume6-
dc.identifier.issue9-
dc.identifier.spage946-
dc.identifier.epage948-
dc.identifier.eissn2159-8290-
dc.identifier.isiWOS:000383356400018-
dc.identifier.issnl2159-8274-

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